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Objective: The objective of this study was to analyse the results of the surgical treatment of coexisting cataract and glaucoma and its effects on corneal endothelial cell density (CECD). Methods: We include two longitudinal prospective studies: one randomised that included 40 eyes with open angle glaucoma that received one- (n= 20) or two-step (n= 20) phacotrabeculectomy and another that included 20 eyes that received phacoemulsification. We assess the impact of surgery on different clinical variables and in particular in CECD using Confoscan 4™ confocal microscopy and semiautomatic counting methods. Results: Phacoemulsification and phacotrabeculectomy, but not trabeculectomy, increase significantly best-corrected visual acuity and anterior chamber depth and trabeculectomy and one- or two-step phacotrabeculectomy decreased similarly the intraocular pressure. We document percentages of endothelial cell loss of 3.1%, 17.9%, 31.6% and 42.6% after trabeculectomy, phacoemulsification and one- or two-step phacotrabeculectomy, respectively. The coefficient of variation did not increase significantly after surgery but the percentage of hexagonality decreased significantly after phacoemulsification and after two-step phacotrabeculectomy. Conclusions: Trabeculectomy, phacoemulsification and phacotrabeculectomy are surgical techniques that cause morphological changes and decrease the densities of the corneal endothelial cells. Trabeculectomy produces lesser endothelial cell loss than phacoemulsification, and phacoemulsification lesser cell loss than phacotrabeculectomy. Two-step phacotrabeculectomy (trabeculectomy followed 3 months later by phacoemulsification) causes more cell loss than one-step phacotrabeculectomy, and this could be due to the cumulative effects of two separate surgical traumas or to a negative conditioning lesion effect of the first surgery. For the treatment of coexisting glaucoma and cataract, one-step phacotrabeculectomy is the treatment of choice.

In adult Sprague—Dawley rats, retinal ganglion cell survival was investigated after intraorbital optic nerve section and after transient ischemia of the retina induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The thickness of the inner nuclear and inner plexiform layers was also assessed after transient periods (120 min) of retinal ischemia induced by selective ligature of the ophthalmic vessels. In addition, we have also investigated the neuroprotective effects of different substances in these paradigms. The intraocular injection of brain-derived neurotrophic factor increased RGC survival after retinal ischemia induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The caspase inhibitor Z-DEVD increased retinal ganglion cell survival after optic nerve section and also after 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. The peptide Bcl-2 did not increase retinal ganglion cell survival after optic nerve section but increased retinal ganglion cell survival after 60 or 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. Finally, BDNF, nifedipine, naloxone and bcl-2 prevented in part the decrease in thickness of the inner nuclear layer and inner plexiform layer induced by selective ligature of the ophthalmic vessels. Our results suggest that retinal ganglion cell loss induced by different types of injury, may be prevented by substances with neuroprotective effects, by altering steps of the cascade of events leading to cell death.